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Overexpression of Cardiac-Specific Kinase TNNI3K Promotes Mouse Embryonic Stem Cells Differentiation into Cardiomyocytes
Wang, Yin ; Wang, Shi-qiang ; Wang, Li-peng ; Yao, Yu-hong ; Ma, Chun-yan ; Ding, Jin-feng ; Ye, Jue ; Meng, Xian-min ; Li, Jian-jun ; Xu, Rui-xia
刊名CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
2017
关键词TNNI3K mESC Differentiation Cardiomyocyte OBESITY-SUSCEPTIBILITY LOCI I-INTERACTING KINASE BODY-MASS INDEX TROPONIN-I PROTEIN IDENTIFICATION EXPRESSION PHOSPHORYLATION CARDIOMYOPATHY HYPERTROPHY
DOI10.1159/000456400
英文摘要Backgroud/Aims: The biological function of cardiac troponin I-interacting kinase (TNNI3K), a cardiac-specific functional kinase, is largely unknown. We investigated the effect of human TNNI3K (hTNNI3K) on the differentiation of mouse embryonic stem cells (mESCs) into cardiomyocytes. Methods: First, the time-space expression of endogenous Tnni3k was detected by real-time polymerase chain reaction (PCR) and western blotting at 16 different time-points over a period of 28 days. Further, action potentials and calcium current with/without 5 mu M nifedipine were measured by patch clamp for mESC-derived cardiomyocytes. HTNNI3K and mouse-derived siRNA were transfected into mESC using lentivirus vector to induce hTNNI3K overexpression and knock-down, respectively. Results: The number of troponin-T (cTnT) positive cells was greater in the group with TNNI3K overexpression as compared to that in control group, while less such cells were detected in the mTnni3k knock-down group as evaluated on flow cytometry (FCM) and ImageXpress Micro system. After upregulation of Connexin43, cardiac troponin-I (Ctni), Ctnt, Gata4 were detected in mESCs with TNNI3K overexpression; however, overexpression of alpha-Actinin and MIc2v was not detected. Interestingly, Ctnt, Connexin40 and Connexin45, the markers of ventricular, atrial, and pacemaker cells, respectively, were detected in by real-time PCR in TNNI3K overexpression group. Conclusion: our study indicated that TNNI3K overexpression promoted mESC differentiating into beating cardiomyocytes and induced up-regulating expression of cTnT by PKCE signal pathway, which suggested a modulation of TNNI3K activity as a potential therapeutic approach for ischemic cardiac disease. (C) 2017 The Author(s) Published by S. Karger AG, Basel; National Natural Scientific Foundation [81100118, 81370203, 81461148026]; Specialized Research Fund for the Doctoral Program of Higher Education of China [20111106110013]; Specialized Research Personnel Fund of Fu Wai Hospital [2012-FWXX02, 2008-F017]; PUMC Youth Fund [2016-XHQN06]; Beijing Municipal Science and Technology Commission [Z141100000214006]; SCI(E); ARTICLE; 1; 381-398; 41
语种英语
内容类型期刊论文
源URL[http://ir.pku.edu.cn/handle/20.500.11897/476043]  
专题生命科学学院
推荐引用方式
GB/T 7714
Wang, Yin,Wang, Shi-qiang,Wang, Li-peng,et al. Overexpression of Cardiac-Specific Kinase TNNI3K Promotes Mouse Embryonic Stem Cells Differentiation into Cardiomyocytes[J]. CELLULAR PHYSIOLOGY AND BIOCHEMISTRY,2017.
APA Wang, Yin.,Wang, Shi-qiang.,Wang, Li-peng.,Yao, Yu-hong.,Ma, Chun-yan.,...&Xu, Rui-xia.(2017).Overexpression of Cardiac-Specific Kinase TNNI3K Promotes Mouse Embryonic Stem Cells Differentiation into Cardiomyocytes.CELLULAR PHYSIOLOGY AND BIOCHEMISTRY.
MLA Wang, Yin,et al."Overexpression of Cardiac-Specific Kinase TNNI3K Promotes Mouse Embryonic Stem Cells Differentiation into Cardiomyocytes".CELLULAR PHYSIOLOGY AND BIOCHEMISTRY (2017).
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